Etiology

Streptococcus pneumoniae (the pneumococcus) is the most common causative pathogen of CAP across a range of severities and patient ages.[8][9][10][11][12] However, other studies have found that influenza virus is the most common cause of CAP in adults.[5][13] In Europe and the US, S pneumoniae accounts for about 30% to 35% of cases.[9][14] The overall incidence rates of pneumococcal CAP in Europe were 68-7000 in 100,000.[15] Other bacterial causes include Haemophilus influenzae, Staphylococcus aureus, and Moraxella catarrhalis.

Atypical bacteria are also common causes, although they vary in frequency depending on the year and any epidemics.[12][16] The incidence of atypical pathogens in CAP is approximately 22% globally, but this varies with location.[17] The most commonly reported atypical bacteria are Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila. M pneumoniae accounts for up to 37% of CAP patients treated as outpatients and 10% of patients who are hospitalized.[9][18]C pneumoniae accounts for 5% to 15% of cases of CAP,[19] and L pneumophila (especially serogroup 1) accounts for 2% to 6% of CAP in immunocompetent patients.[20] A systematic review found that Chlamydia psittaci was the causative organism in 1% of patients.[21] However, a Dutch study identified C psittaci by polymerase chain reaction (PCR) of sputum (when available) as a cause of CAP in 4.8% of cases.[22]

Approximately 6% of cases are due to PES pathogens (Pseudomonas aeruginosa, extended-spectrum beta-lactamase Enterobacteriaceae, and methicillin-resistant S aureus [MRSA]). Of these organisms, P aeruginosa and MRSA are the most frequently reported.[23][24]

Respiratory viruses are reported in about 10% to 30% of immunocompetent adults hospitalized with CAP.[9][25][26][27] Influenza virus A/B, respiratory syncytial virus, adenovirus, rhinovirus, and parainfluenza virus are the most common viral causes of CAP in immunocompetent adults. Viral sepsis has been reported in 3% of all patients admitted to the emergency department with a diagnosis of CAP, 19% of all patients with CAP who are admitted to the intensive care unit, and 61% of those with a diagnosis of viral CAP. Males and older patients (age ≥65 years) are at an increased risk for viral sepsis.[28] Newer pathogens reported to cause CAP include metapneumovirus and coronaviruses.[29] Detection of viral causes is increasing because of the use of PCR.

Polymicrobial etiology in CAP varies from 5.7% to 13.0%, depending on the population and the microbiological diagnostic test used.[9][26][30]

Pathophysiology

Pneumonia develops subsequent to the invasion and overgrowth of a pathogenic microorganism in the lung parenchyma, which overwhelms host defenses and produces intra-alveolar exudates.[31]

The development and severity of pneumonia is a balance between pathogen factors (virulence, inoculum size) and host factors. The likely microbial causes of CAP differ according to a number of factors, including differences in local epidemiology, the setting (outpatients, hospitalized, or intensive care unit), severity of disease, and patient characteristics (e.g., sex, age, and comorbidities).[9]

Microbes that are present in the upper airways can enter the lower airways by microaspiration. Nevertheless, the defense mechanisms of the lungs (innate and acquired) keep the lower airways sterile. The development of pneumonia indicates a defect in host defenses, exposure to a particularly virulent microorganism, or a large inoculum size.

Impaired immune response (e.g., caused by HIV infection or advanced age) or dysfunction of defense mechanism (e.g., through current or passive smoking, COPD, or aspiration) leads to greater susceptibility to respiratory infections in patients.[32]

Pathogens can reach the lower respiratory tract by 4 mechanisms:

  • Inhalation, a common route of entry for viral and atypical pneumonia in younger healthy patients. Infectious aerosols are inhaled into the respiratory tract of a susceptible person to initiate infection

  • Aspiration of oropharyngeal secretions into the trachea, the primary route through which pathogens enter the lower airways

  • Hematogenous spread from a localized infected site (e.g., right-sided endocarditis)[33]

  • Direct extension from adjacent infected foci (e.g., tuberculosis can spread contiguously from the lymph nodes to the pericardium or the lung, albeit rarely).

Pneumonia may result from dysbiosis of the normal lung flora, rather than invasion of pathogenic microorganisms in a sterile environment.[34] Multiple bacterial species (e.g., Prevotella, Veillonella, Streptococcus, Fusobacterium, and Haemophilus) are present in a healthy lung and are known as the lung microbiome. The upper respiratory tract is the primary source of the lung microbiome. These bacteria are part of a dynamic community where a balance, or equilibrium, is maintained. When disequilibrium (or dysbiosis) occurs, as is the case in acute infections, the microbiome changes. Risk factors for dysbiosis are partially understood, but further study is required.[35][36]

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